ACUTE NONSPECIFIC BACK PAIN
Nonspecific back pain is a symptom complex that has countless names, including back strain/sprain, mechanical back pain, and lumbago. However, because strain and/or sprain have no histopathologic findings, a more accurate term to use is idiopathic or nonspecific back pain. Nonspecific back pain is the authors' choice of term, especially because most patients will never be given a more precise diagnosis.
Diagnosis is clinical. The pain is mild to moderate and is aggravated with movement and relieved with rest. Although the typical mechanism is usually minor exertion or lifting, the patient may not recall any remarkable etiology. There are no risk factors for serious disease on the history and physical examination, or if any risk factors are present, the diagnostic evaluation is normal.
Treatment focuses on restriction of activity, analgesia, manipulation, and other physical modalities. Monitor symptoms for 4 to 6 weeks before embarking on further diagnostics. In 80% to 90% of patients, symptoms will resolve on their own within this time period.15 Watchful waiting avoids wasting time and money and eliminates exposure to unnecessary radiation. This course of action should be discussed with patients because they may expect diagnostic testing.
Patients who resume their normal activities to the furthest extent tolerable recover more rapidly than those on 2 or 7 days of bed rest or those who perform back-mobilizing exercises.23 Thus, patients should continue daily activities using pain as the limiting factor.15 Withhold exercise programs until the acute painful episode has resolved or improved significantly.
Medication is a combination of acetaminophen and NSAIDs. Acetaminophen is an excellent first-line agent, and there is little evidence that NSAIDs are more effective for symptomatic relief.24,25 Most NSAIDs are equally efficacious for back pain. However, there are significant differences in the side effect profiles and toxicity. In one review, ibuprofen was the least toxic of the 12 NSAIDs studied, particularly with regard to upper GI bleeding. Because there is a linear relationship between dose and toxicity, the lowest dose possible should be used in patients at risk. In patients at risk for GI bleeding, the addition of a proton pump inhibitor or misoprostol can reduce the risk.25
We recommend using acetaminophen in combination with NSAIDs or as the sole initial agent when treating patients at higher risk for adverse effects of NSAIDs (the elderly and those with renal disease or peptic ulcers). One regimen is acetaminophen, 650 to 975 milligrams every 4 to 6 hours (do not exceed 4 grams in a 24-hour period), either alone or in conjunction with ibuprofen, 800 milligrams three times daily, or naproxen, 250 to 500 milligrams twice daily. If there is a concern for GI bleeding, then add a proton pump inhibitor such as omeprazole, 20 milligrams once daily.
Opioid analgesics should be offered to patients with moderate to severe pain, but for a limited (1 week) duration, as they are only effective in the short term.15,24,26 When prescribing opioid analgesic combinations that include acetaminophen, warn patients not to combine them with other acetaminophen products.
Muscle relaxants are useful for treating back pain.26 Muscle relaxants, such as diazepam, 5 to 10 milligrams every 6 to 8 hours, and methocarbamol, 1000 to 1500 milligrams four times a day, are effective. Although their efficacy appears equal to NSAIDs, there are no studies comparing muscle relaxants alone with NSAIDs in the treatment of nonspecific low back pain. Additionally, there does not appear to be any additional pain relief or synergistic benefit when these medications are used in combination.27 Corticosteroids taken systemically or injected locally or into the epidural space have no role in the treatment of nonspecific back pain.15,28
Manipulative therapy, while not generally an ED treatment, is one of the more controversial treatment options for back pain. Clinical outcome of manipulation is no better than standard medical therapy according to a Cochrane review,29 but is not harmful.15
Other physical modalities include traction, diathermy, cutaneous laser treatment, exercise, US treatment, and transcutaneous electrical nerve stimulation. None of these have any proven efficacy in the treatment of acute low back symptoms. The application of heat or ice may provide temporary symptomatic relief in some patients, with evidence favoring heat.15
CHRONIC NONSPECIFIC BACK PAIN
There is a higher concern for serious disease in patients with ongoing or intermittent symptoms for a time period of months to years. The best approach is to review the previous evaluations for completeness and to be sure that abnormalities were not overlooked. If the evaluation has been incomplete, then consider completing it in the ED at that visit, or facilitate referral for an outpatient evaluation, with urgency guided by the severity of symptoms. If the evaluation has been thorough but negative, then treat as described for nonspecific back pain. If opioid analgesics are needed, prescribe them for only a very limited time. Chronic back pain is a difficult condition to manage, and benefit of medications is small.15,24,26,30 Further information on the management of chronic back pain can be found in chapter 38.
LOW BACK PAIN WITH SCIATICA
Although sciatica only affects a very small proportion of all patients with back pain, it is present in the vast majority of patients with a symptomatic herniated disk. Although disk herniation is the most common cause of sciatica, anything that compresses or impinges on the spinal nerve roots, cauda equina, or spinal cord can cause sciatica. Other important etiologies to consider in the ED include intraspinal tumor or infection, foraminal stenosis, extraspinal plexus compression, piriformis syndrome (see chapter 281, "Hip and Knee Pain"), and lumbar canal stenosis (spinal stenosis).
Diagnosis is suspected clinically and confirmed with nonurgent MRI (urgent MRI only in the setting of suspected spinal cord compression). Patients who present with sciatica due to a herniated disk generally complain more about the radicular symptoms than about back pain. Because the vast majority of disk herniations occur at the L4-L5 (L5 nerve root) or L5-S1 (S1 nerve root) level, the radicular pain extends below the knee in the dermatomal distribution of that nerve root. A small proportion (often the elderly) have disk herniation at the L2-L3 (L3 nerve root) and L3-L4 (L4 nerve root) levels. The physical examination generally demonstrates localization of pain and a neurologic deficit in a unilateral single nerve root, usually L5 or S1, and frequently includes a positive result on straight leg raise testing.
If the patient has no risk factors in the history and physical examination for serious disease other than sciatica, treat conservatively and do not perform any diagnostic tests in the ED.15 If the patient has a demonstrable neurologic deficit, consider obtaining plain radiographs to look for other possible causes for symptoms such as tumor, fracture, spondylolisthesis, and infection. Guidelines recommend imaging (MRI preferred) in patients with severe or progressive neurologic deficits and those with serious underlying conditions suspected based on history or physical examination.15 If the symptoms have not progressed rapidly or the symptoms are not severe, the MRI can be ordered routinely or urgently rather than emergently.
Treatment is as for nonspecific back pain. Routine daily activity is as good as 2 weeks of bed rest in terms of intensity of pain, distress associated with symptoms, and functional status.23 Recommendations for analgesic (acetaminophen, NSAID, and opiates) and muscle relaxant therapy remain the same.31 NSAIDs are less effective in treating the symptoms of a herniated disk than they are in treating nonspecific back pain.
Corticosteroid therapy for herniated disk has limited benefit. Specifically, epidural corticosteroid injection provides a minor reduction in leg pain and sensory deficits in comparison with placebo. However, the improvement in symptoms is not associated with any significant functional benefit, and it does not reduce the need for surgery. Although epidural steroid injection is not an ED procedure, it offers an alternative for the moderately to severely symptomatic patient in follow-up. Although oral steroids are used widely, they appear to have little measurable benefit in patients with sciatica.
Manipulation is not recommended for the routine management of symptoms from herniated disk.29 Local application of heat or ice may provide temporary relief.
Most patients with a herniated disk may be treated and monitored by their primary care physician without specialist referral. Most patients ultimately improve with nonsurgical therapy, with over half recovering in 6 weeks. Most spine surgeons agree that surgery is appropriate only when all three of the following criteria are met: definitive evidence of herniation on imaging study; corresponding clinical picture and neurologic deficit; and conservative treatment for 4 to 6 weeks that fails to produce improvement.
Emergency decompressive surgery is required only in patients with acute epidural compression syndromes. Patients who underwent surgery had improved function and fewer symptoms at 1 and 2 years postoperatively, compared with those treated conservatively; however, by 4 and 10 years postoperatively, both groups had comparable results.32,33
Spinal stenosis is a narrowing of any part of the lumbar spine, including the spinal canal, nerve root canal, and intervertebral foramina, which may occur at single or multiple spinal levels. Degenerative disease causes narrowing and compression of vascular and neural structures. It is a cause of chronic back pain, with or without associated sciatica. The symptoms, which usually begin in the sixth decade, include low back pain that is aggravated by prolonged standing and spinal extension and is relieved by rest and forward flexion. Typically, symptomatic patients present with low back and lower extremity pain while walking that is symptomatically similar to vascular claudication. This symptom is termed neurogenic claudication or pseudoclaudication to distinguish it from vascular claudication. Neurogenic claudication is relieved with rest and forward flexing the spine and worsened by extending the spine.34 Physical examination findings are often absent. The diagnosis is made principally by history with confirmation by CT scan or MRI. Symptomatic treatment is the same as chronic back pain with primary care follow-up.
Ankylosing spondylitis is an autoimmune arthritis that primarily affects the spine and pelvis. It is associated with human leukocyte antigen B-27, trauma, and infection. It most commonly occurs in patients <40 years old with a 3:1 male predilection. Patients complain of awakening with low back pain and stiffness that improves throughout the day with mild activity. The diagnosis is suspected by history and physical exam in individuals with symptoms longer than 3 months in duration and is confirmed by imaging and laboratory tests. Radiographic studies demonstrate sacroiliitis and squaring of the vertebral bodies, the so-called bamboo spine. Patients can be treated symptomatically with NSAIDs and should be referred to a rheumatologist for diagnostic confirmation and further management.
EPIDURAL COMPRESSION SYNDROME
Epidural compression syndrome is a collective term encompassing spinal cord compression, cauda equina syndrome, and conus medullaris syndrome.
Although the diagnosis of a complete epidural compression is obvious, the challenge is diagnosis in patients with early signs and symptoms. The initial differential diagnosis is broad and includes most conditions that cause weakness, sensory changes, or autonomic dysfunction of the lower extremities. The history and physical examination should narrow the differential diagnosis to a compressive lesion of the spinal cord or cauda equina.
Possible causes of epidural compression include spinal canal hemorrhage with hematoma, tumors of the spine or epidural space, spinal canal infections including spinal epidural abscess, and massive midline disk herniation. Transverse myelitis is a noncompressive condition that may present clinically like a compressive lesion of the spinal cord.
The history usually includes back pain with associated neurologic deficits. Specifically, it may include perianal sensory loss, fecal incontinence or urinary incontinence with or without retention, and sciatica in one or both legs. The duration of symptoms does not differentiate these syndromes from benign causes of back pain. In one small study, urinary retention of >500 mL alone or in combination with two of the following characteristics—bilateral sciatica, subjective urinary retention, or rectal incontinence symptoms—is the most important predictor of MRI-confirmed cauda compressions.35 Also, a history of malignancy and a rapid progression of neurologic symptoms, especially bilateral symptoms, increase the likelihood of compression.
The physical examination findings vary depending on the level of compression and the amount and area of the spinal cord or cauda equina that is compressed. The most common finding in cauda equina syndrome is urinary retention with or without overflow incontinence, with a sensitivity of 90% and a specificity of about 95%.35 Other common findings for epidural compression include weakness or stiffness in the lower extremities, paresthesias or sensory deficits, gait difficulty, and abnormal results on straight leg raise testing.36 The most common sensory deficit occurs over the buttocks, posterosuperior thighs, and perineal regions and is commonly called saddle anesthesia. Anal sphincter tone is decreased in 60% to 80% of cases.
When one clinically suspects epidural compression, especially due to tumor, treat the patient with dexamethasone, 10 milligrams IV, before obtaining any confirmatory tests.36 After the patient has received dexamethasone, obtain an emergent MRI of the spine. If investigating the possibility of epidural compression due to neoplasm, obtain an MRI of the entire spine because 10% of patients with vertebral metastases have additional silent epidural metastases that would be missed by a localized imaging study.36 The presence of tumors remote from the symptomatic site may change patient management. Additionally, the neurologic examination may falsely localize the spinal lesion(s) and limited regional MRI may not detect the lesion. If one suspects a pure cauda equina syndrome from a herniated disk, then it is reasonable to obtain an MRI localized to the lumbosacral spine.
The functional clinical outcome for epidural compression from tumor depends on patient symptoms at presentation. Patients who cannot walk before treatment rarely walk again. Those who are too weak to walk without assistance but who are not paraplegic have a 50% chance of walking again. Those who are able to walk when treatment begins are likely to remain ambulatory.36 Of those patients who require a catheter for urinary retention before treatment, 82% will continue to require the urinary catheter after treatment. The presence of cord compresion is an indication for urgent consultation with a spine surgeon for decompression and/or radiation therapy for a tumor mass, determined by MRI findings.37,38
Transverse myelitis is an inflammatory disorder that involves a complete transverse section of the spinal cord. It usually presents with neck or back pain in association with neurologic complaints and findings on physical examination, depending on the level of the spinal cord that is involved. The typical clinical syndrome involves bilateral motor, sensory, and autonomic disturbances that may progress over a period of days to weeks. Fecal and urinary retention and incontinence are common.39 Transverse myelitis may result from viral infection, after vaccination, or as part of a systemic disease such as systemic lupus erythematosus, cancer, or, more commonly, multiple sclerosis. The most important issue regarding transverse myelitis is recognition of the potential for a compressive lesion of the spinal cord and managing the patient as outlined under epidural compression syndromes. The MRI may demonstrate lesions of the spinal cord, but MRI findings may lag the clinical presentation, especially early in the disease process.38 In those situations where the patient has definite neurologic findings that are consistent with epidural compression but has a normal MRI, transverse myelitis is one of the primary working diagnoses. In such cases, consult a neurologist for admission and consider performing a lumbar puncture to assist in the diagnosis. The spinal fluid most commonly demonstrates lymphocytosis and elevated protein.38 Treatment includes corticosteroids and plasma exchange at the direction of a neurologist.38
Spinal infections, such as vertebral osteomyelitis, discitis, and spinal epidural abscess, are uncommon but serious causes of back pain. Unfortunately, these infections are commonly missed on first assessment.19,22 Risk factors for infection include the following: immunocompromised states (diabetes, HIV infection, and organ transplant recipients), alcoholism, recent invasive procedures, spinal implants and devices, injection drug use, and skin abscesses.16,19,22
Patients with vertebral osteomyelitis usually have had prolonged symptoms, and in many cases, pain has been present for >3 months.19,40 On physical examination, about half have fever and vertebral body tenderness to percussion.19,40 The WBC may be normal, but the erythrocyte sedimentation rate and C-reactive protein are almost always elevated, although this is nonspecific.16,17,19,40 Blood cultures are positive in approximately 40% of cases of vertebral osteomyelitis and should be routinely drawn as part of the management. In osteomyelitis, plain radiographs are normal until the bone demineralizes, which can take from 2 to 8 weeks. The most common radiographic abnormalities with vertebral osteomyelitis are bony destruction, irregularity of vertebral end plates, and disk space narrowing.19 See the section on osteomyelitis in chapter 281 for further discussion.
In patients with discitis, >90% present with a complaint of unremitting back or neck pain, which awakens them at night and is relieved by neither rest nor analgesics.19 Fever is present in 60% to 70% of patients, whereas the percentage of patients with neurologic deficits is highly variable, from 10% to 50%.19 Elevation in the erythrocyte sedimentation rate occurs in >90% of patients, whereas elevated WBC count occurs in less than half of patients.19
The classic triad of symptoms suggesting spinal epidural abscess is severe back pain, fever, and neurologic deficits, but the triad occurs in only 8% to 13% of patients.22 Spinal epidural abscess is commonly found in association with vertebral osteomyelitis and discitis, in 62% and 38% of cases, respectively.16,22 Risk factors 98% sensitive for epidural abscess include injection drug use, immunocompromise, alcohol abuse, recent spine procedure, distant site of infection, diabetes, indwelling catheter, recent spine fracture, chronic renal failure, and cancer.22 Erythrocyte sedimentation rate is elevated (>20 mm/h) in >95% of patients,16,17,22 and the C-reactive protein is elevated in >90% of patients.19 For all spinal infections, contrast-enhanced MRI is the gold standard imaging study. For detailed discussion, see chapter 174, "Central Nervous System and Spinal Infections."
Treatment of Spinal Infections
Epidural abscess requires antibiotics and emergent evaluation and treatment by a spine surgeon. The treatment for discitis is long-term antibiotics, with surgery reserved for those with spinal cord compression or biomechanical instability. The treatment for vertebral osteomyelitis is primarily medical, consisting of 6 weeks of IV antibiotics followed by a 4- to 8-week course of oral antibiotics. For vertebral osteomyelitis, consult with a spine surgeon before antibiotic administration, because antibiotics may result in negative culture results from a bone biopsy. However, do not withhold antibiotics unless specifically directed by the spine surgeon. Empiric antibiotic therapy should be directed against Staphylococcus aureus. Parenteral piperacillin-tazobactam, 3.375 grams IV, and vancomycin, 1 gram IV, or similar agents with broad-spectrum coverage can be given until culture results are available.17,18 The remainder of treatment is symptomatic.